to explain it. On the one hand, it has been said the fibrin pre-exists
in the blood, and by the fact of the slowing of the circulation, the
reduction of the {722} temperature, etc. the fibrin separates from the
blood and coagulates. Again, it is admitted that the fibrin does not
exist formed in the blood, but that a fibrinogenous material is present
which is acted upon by the hæmoglobin or globulin contained in the red
globules, the leucocytes, and the corpuscles of connective tissue, and
sometimes is, sometimes is not, caused to precipitate as fibrin
(Virchow). The exact conditions which occasion the activity of the
globulin are unknown. The reaction which takes place has been said to
resemble that which takes place between amygdalin and emulsin when
prussic acid is formed, or between myrosin and myronic acid when the
volatile oil of mustard is produced. Further, it is stated, in
accordance with accurate chemical investigations, that the plasma of
the blood contains a substance called plasmin, which separates itself
into fibrin which coagulates and into fibrin which remains dissolved in
the blood (metalbumen, Robin). These fibrins are evidently of two
kinds. The plasmin divides itself under the influence of slowing of the
circulation, the action of acids, of foreign bodies, of oxygen in
excess, etc.; it remains intact in a fluid condition when the vascular
walls and globules are healthy, the blood circulating with normal
rapidity, and in presence of alkaline principles.[8] According to
Foster,[9] "Coagulation is the result of the interaction of two bodies,
paraglobulin and fibrinogen, brought about by the agency of a third
body, fibrin ferment." Schmidt concludes that when blood is shed a
number of white and intermediate corpuscles fall to pieces, by which
act a quantity of fibrin ferment and of paraglobulin is discharged into
the plasma. These meeting there with the already present fibrogen give
rise to fibrin, and coagulation results.
[Footnote 8: _Dict. de Méd. et de Chirurgie pratique_, vol. viii. p.
569.]
[Footnote 9: _A Textbook of Physiology_, p. 22, New York, 1880.]
As regards the formation of clots within the body, it is supposed that
injured or diseased spots or foreign bodies first attract, and then, as
it were, by irritation cause the death of, a certain number of
corpuscles.[10] The views of Schmidt of the fibrino-plastic function of
paraglobulin are not accepted by all investigators; and some authors
believe that the fibrinogen as well as the fibrin ferment arises from
the white corpuscles.[11]
[Footnote 10: _Pflüger's Archiv_, vi. (1872), p. 413; xi. (1875), pp.
291 and 515; xiii. (1876), pp. 93 and 146; quoted by Foster.]
[Footnote 11: Frédericq, L., _Recherches sur la Coagulation du Sang_,
Bruxelles, 1877, quoted by Foster.]
According to Bristowe,[12] the frequency of sanguineous concretions
does not depend upon sex, but is in a certain relation with age. He has
remarked, for example, that they are proportionately more often met
with at the extremes of life than toward middle age. This might be
explained satisfactorily, perhaps, on the supposition that at these
periods the circulation is at times very feeble, owing either to
congenital feebleness on the one hand or chronic organic affections on
the other. At all events, when we seek for the causes which have most
influence in determining the formation of cardiac concretions previous
to death, we find--I. the mechanical, or those which act specially in
slowing the current of blood through the heart. These causes may exist
within the heart or may be removed from it. II. The vital or
pathological. These causes are of somewhat difficult determination at
times, and pertain usually to affections in which there is notable
blood-change, in which the quantity of the fibrin has been augmented
absolutely or relatively, or to those of infectious type--viz.
diphtheria; or to those constitutional in nature--phthisis, cancer,
etc. III. The inflammation of the endocardium or endocarditis. This is
admitted by Andral, in a note upon the etiology of cardiac concretions
in the work of Laennec, as having special importance. Bouillaud also
attributed their formation in certain cases to the chemical action of
pus which was present in the economy.
[Footnote 12: _Pathol. Society's Trans._, vol. xiv. p. 71, quoted by
Bartholow.]
{723} I. Amongst the mechanical causes we should mention all organic
lesions of the heart, all obstacles in the pulmonary circulation, and
possibly, by analogy, certain badly-defined lesions of the
pneumogastric nerves. All the stenoses and dilatations of orifices, all
irregularities of the valves or heart-walls, all depressions or
roughened parts of the walls,[13] may determine the beginning of a
concretion. In the same way, a small mass of fibrin deposited on a
calcareous valve after transport from one of the veins of the limbs may
originate a voluminous heart-clot. Dilatation of the heart,
pericarditis, every cardiac change which weakens the contractile power,
is a predisposing cause of cardiac thrombosis. Every organic lesion of
the heart tending toward that final stage of asystolism so often
encountered, and which weakens so greatly cardiac contractility;
pouching of different portions of the cardiac wall, or aneurism;
pressure upon the right heart by a mediastinal tumor or a sacculated
aneurism of the arch of the aorta,[14]--all these have great power in
producing intra-cardiac thrombi. The mechanism of these different
lesions was familiar to Kreyssig, Laennec, and Hope. At the same time
it must be admitted that these changes in the heart are not of
themselves always sufficient to give rise to fibrinous deposits. We
encounter stenoses and regurgitations at orifices very frequently, and
concretions, on the other hand, are relatively rare. Moreover, we find
heart-clot at times when there is no cardiac alteration. We believe,
therefore, that the heart lesion is an aiding factor--that in the last
moments of life, when the force of the heart's contraction is weakened
and the conditions of the blood favor coagulation, they will act with
special power.
[Footnote 13: _Pathol. Society's Trans._, vol. xiv. p. 71, cases by J.
W. Ogle.]
[Footnote 14: Walshe, _Dis. of the Heart_, Lond., 1873.]
Among the mechanical causes which are removed or distant should be
mentioned all those which interfere with the pulmonary circulation.
Such are the effects left behind by pneumonia, pleuro-pneumonia, or the
compression of the blood-vessels by old congestion of the lungs. In
these cases, when the vis a tergo is impaired somewhat, and an obstacle
is placed in the pulmonary capillary circulation, even if cardiac
thrombosis does not directly result at first, we may have thrombi form
in the pulmonary veins. In the same way, the nervous affections which
are accompanied with slowing of the circulation tend to produce
coagulation of the blood. All lesions, as we have said, of the
pneumogastrics act in the same direction. In proof of this we should
cite the experiments of Meyer of Bonn, of Longet, and of Blondet, who
produced fibrinous concretions in the hearts of animals by tying or
cutting the pneumogastric nerves. At the same time, the heart-beats
became more rapid, wavering, unequal, and less energetic than in
ordinary physiological conditions. After all, however, all these
mechanical causes are but predisposing causes, for they do not always
produce cardiac concretions. Frequently, as we have said already, the
obstruction to the circulation may be present, and yet at the autopsy
no fibrinous deposit be found in the heart. In order that the
mechanical causes act efficiently to produce coagula, it is essential
that they be aided by the conditions of the blood which favor it.
All concretions do not form with the same rapidity nor are they of the
same size. At times their production is sudden, and but a few hours
elapse before the fatal termination is reached. Again, it is affirmed
that weeks, and even months, may pass before the concretion has reached
a volume sufficient to cause entire stoppage of the heart's
contractions. In the former category are found, of course, the softer,
least consistent coagula--usually, however, very voluminous; in the
latter are the smaller, more elastic, and resistant concretions, at
times even presenting a stratified structure[15] and {724} surrounded
habitually by a clot formed during the latter moments of life, and
having a large proportion of cruor in its composition. The heart
affected with fatty degeneration should, if we consider its weakened
power and deficient contractility, be a predisposing cause of
stagnation first, and finally of the formation of intra-cardiac
thrombi. As a matter of observation in the dead-house, however, such
hearts are not frequently accompanied with fibrinous deposits in their
cavities.
[Footnote 15: According to Legroux, roughening of the walls or valves
gives rise to stratified coagula of moderate size, or else to those
small clots which deposit on the surface or margin of the valves
(_Dict. Encycl. des Sci. méd._, article "Concrétions sanguines," Paris,
1876).]
All diseases which by their nature and duration produce great
exhaustion of the vital powers tend strongly to produce fibrinous
coagula in the heart. This is eminently true of those which at the same
time do not occasion a diminished plasticity of the blood. It is often
assumed that mere stasis in the blood-current through the heart is
essential to the formation of clots in its cavities, and to lend
support to this belief reference is made to the phenomena which take
place in bleeding. It is not true, however, that stasis is necessary to
coagulation, and the proof is afforded when we take a bundle of twigs
and by beating the blood forcibly produce the separation of the fibrin.
Besides a slowness of the circulation, there must be, once again, an
obstacle in the heart itself, and even then polypoid concretions are
not always formed.[16]
[Footnote 16: _Gaz. hébdomadaire_, Paris, 1856.]
II. The Vital or Pathological Causes.--In this class of conditions
leading to cardiac thrombosis are included all diseases in which
certain special changes have taken place in the blood itself. Among
these we should mention, first, certain sthenic inflammatory affections
in which the proportion of the plasmin (fibrin and metalbumen) is
notably elevated, and in which, on this account, there is a strong
tendency to the separation of fibrin from the blood and to the
formation of cardiac concretions. In fibrinous pneumonia and acute
rheumatism this is particularly true, and amongst the numerous
accidents we have to dread in the course of these diseases none strike
us with more dread than the possible production of intra-cardiac
thrombi. In fibrinous pneumonia this complication is so frequent that
Bouillaud has enunciated the following pathological law: "Fibrinous
concretions exist constantly in patients who succumb to a frank, acute
pleuro-pneumonia, well characterized, which has reached the second
stage."[17] According to Raynaud, this is without question a great
exaggeration, and results from the confusion this learned author
evidently made between terminal clots and those formed some time
previous to death. Nevertheless, there is here a proof of the great
frequency of coagula occasioned by this disease, and of the strong
tendency to their formation which the condition of the blood must
afford. What we have said of fibrinous pneumonia and acute articular
rheumatism is not true, singular to say, of lobular or
broncho-pneumonia. The lesions of this form of pneumonia are those of a
catarrhal inflammation of the lung, and the blood does not offer during
its course the remarkable tendency to coagulation that is shown in
fibrinous pneumonia. Usually, the heart-cavities and the vessels are
filled after death with a liquid of a black or violet-brown color, very
often sticky.[18] The fibrin in the heart-cavities in pneumonia is
fibrillar, and does not present those changes which indicate that it
has been deposited for a long while. Moreover, these coagula do not
present physical characters which show any considerable degree of age.
They are usually terminal coagula, or at least formed within a few days
of the fatal termination. Do globular vegetations occur in pneumonia?
At times they do, but they are at least very rare as compared with the
fibrinous conditions just referred to.
[Footnote 17: _Gazette méd._, 1843, vol. xi. p. 270, quoted by Armand,
_Thèse de Paris_, 1857, p. 41.]
[Footnote 18: Damaschino, _Thèse de Paris_.]
There are other general conditions in which there is a marked tendency
to {725} the formation of cardiac coagula. In the puerperal state,
according to Simpson, it is occasioned by the resorption of many new
elements which vitiate its composition and thus occasion this result.
In the poisoning following upon glanders or pyohæmia intra-cardiac
thrombi are often found. Lancereaux has found in this latter disease
fibrinous deposits in the right ventricle and pulmonary artery around
small masses composed of pus-cells. In the different cachectic states,
such as those caused by chronic Bright's disease,[19] advanced
phthisis, and cancer, although we have a diminution in the proportion
of red globules, there is present at the same time a relative increase
of fibrin; and the consequence is that concretions are often formed in
the heart. In fact, it is in these cachexiæ that we often encounter
those fibrinous cysts which will be described under the title of Morbid
Anatomy.
[Footnote 19: Here the retention of the excreta is an important factor
in the formation of cardiac thrombosis (Bristowe).]
Many well-known authors have declared that diphtheria was very powerful
in producing fibrinous concretions in the right heart some time
previous to death. Among those who have written specially on this
subject we would mention Winkler,[20] Richardson,[21] Meigs[22] and
Robinson.[23] According to the latter writer, elastic fibrinous clots
twisted in the valves and adherent to the cardiac walls are developed
frequently in children at a period quite removed from that of the
agony, and at a time when they are not as yet in a condition of extreme
weakness. Except in exceptional instances this influence of diphtheria
to produce cardiac coagula is doubted by Parrot.[24] He admits its
power, particularly when it is complicated with membranous croup, and
in these examples he believes the precocious formation of coagula is
determined probably by the asphyxic condition. Whilst denying the
influence of diphtheria, Parrot freely acknowledges that measles,
especially when complicated with broncho-pneumonia, tends to produce
cardiac concretions. The same tendency is recognized by Harley in the
early stage of scarlet fever where there is high pyrexia.[25]
[Footnote 20: _Die Bluthlumpen dann der Häutiger Bräune_, Wien, 1852.]
[Footnote 21: _Med. Times_, vol. i. p. 23, 1860.]
[Footnote 22: _Am. Journ. Med. Sci._, April, 1864.]
[Footnote 23: _De la Thrombose cardiaque dans la Diphthérie_, Paris,
1872.]
[Footnote 24: _Dict. Encycl. des Sci. méd._, vol. xviii. p. 484.]
[Footnote 25: _Medico-Chirurg. Trans._, vol. lv.]
Notwithstanding the diminished proportion of fibrin in typhoid fever,
and the impossibility of explaining, in many cases, any increase of the
plasticity by local inflammatory disorders, cardiac concretions have
been observed by Huss, Virchow, and Hardy.[26] Bucquoy also relates,
after Huxham, an epidemic which reigned at Plymouth in 1742 amongst
sailors who came from a long cruise, characterized by dyspnoea, cardiac
palpitations, and intermittences of the pulse. Many of those attacked
died, and at the autopsies made polypoid concretions of considerable
elasticity and adherent to the walls of the heart were found. Another
similar occurrence took place amongst the soldiers of the garrison of
Rocroy in 1746. Quite a number succumbed after having shown symptoms
similar to those of the sailors of Huxham. Cadaveric sections
discovered in the left ventricle several hard, consistent cardiac
thrombi.
[Footnote 26: Quoted by Bucquoy, _Des Concrétions sanguines_, Paris,
1863, p. 36.]
III. Endocarditis.--Whatever may be the opinion of different authors in
regard to the frequency of endocarditis when intra-cardiac thrombi are
present, it is certain that if it does exist the explanation of the
presence of these deposits is clear and ample. In endocarditis we have
both a local and mechanical cause and also a vital condition of
fibrinous deposits in the heart. As a mechanical cause we know that
often it is the cause of the stenoses of orifice which are present, and
that further, by its effect in producing roughening or fissuring of
surface, it offers a strongly predisposing cause of the {726} deposit
of fibrin. Ulcerative endocarditis acts still more efficiently in this
direction, owing to the fact that it produces its effects as much on
the surface of the valve, aortic and mitral, near the adherent portion
and in the neighborhood of the cardiac orifice, as between its layers.
The result is, that the surface is rough, unequal, presenting often
cauliflower excrescences, and showing sometimes, in the midst of a mass
of fibrin that has become deposited by degrees, portions of a softened,
partially-detached valve which was the nucleus of the outer layers of
fibrin. Further, endocarditis of both forms acts as a vital and
efficient cause of cardiac thrombosis, in that it belongs to the class
of inflammatory diseases which occasions an absolute increase in the
proportion of fibrin of the blood (from 25/1000, concrete fibrin 3, and
metalbumen 22, to 56/1000, concrete fibrin 17, metalbumen 36); and
also, more especially in ulcerous endocarditis, by the transport of
infectious materials into the blood, which still further tend to cause
coagulation.[27]
[Footnote 27: At times there is complete deprivation of epithelium over
a limited area, and in rare cases slight ulcerations of membrane. These
two conditions are efficient factors of the exudation of plastic
lymph.]
SYMPTOMATOLOGY.--According to Laennec,[28] it is equally erroneous to
attribute to cardiac thrombosis many symptoms which properly belong to
an organic lesion of the heart (notably hypertrophy) as it is to
believe that intra-cardiac thrombi never begin to form until the
terminal period of life. According to him, Haller, Vinckler, Staneari,
and Bonaroli[29] have observed obliterations of the internal jugular
vein and carotid artery by very firm concrete fibrin, and he himself
has seen a similar production in the inferior vena cava for the space
of four fingers' breadth. Although these concretions were evidently
formed during life, they occasioned no symptoms indicative of their
presence, nor were there any obstructions in the course of the
circulation which could explain their origin. Reasoning from these
facts and from the phenomena which occur in aneurismal tumors, it seems
highly probable that the blood should coagulate in the heart also
during life. Later writers frankly admitted that coagulations in the
veins caused partial dropsies, a usual instance of which is the white
swelled leg, or phlegmasia alba dolens, from obliteration of the
femoral vein.[30] This is not invariable, for I have seen, in patients
who have succumbed to diphtheria, both venæ cavæ obstructed by coagula,
without having observed during life either local or general oedema.[31]
[Footnote 28: _A Treatise on Diseases of the Chest_, p. 183, Philada.,
1823.]
[Footnote 29: Quoted by Morgagni, _Epist._ 64.]
[Footnote 30: Vide Bouillaud, _Archiv. gén. de, Méd._, t. ii. et v.,
quoted by Hope.]
[Footnote 31: _Thrombose cardiaque dans la Diphthérie_, Paris, 1872, p.
43.]
Scarcely any contemporary author doubts that cardiac thrombosis gives
rise to more or less well-defined symptoms. What these are we shall now
consider. Of course we are far less liable to-day, when the diagnosis
of organic cardiac disease is so accurate, to attribute to
intra-cardiac thrombi the signs, physical or rational, which properly
belong to them, and which ancient observers could not differentiate.
Nevertheless, there are complex cases in which one is at fault even in
regard to this problem.
The symptoms of cardiac thrombosis vary naturally with their size,
situation, and rapidity of formation. Certain authors have affirmed,
for example, that the concretions formed in an auricle cause a greater
amount of interference with the circulation than those elsewhere
situated. This they do partly by reason of their size and the less
contractile power possessed by the auricle, partly because from the
auricle prolongations are sent off which occlude the cardiac orifices.
When cardiac concretions form suddenly a few days previous to death,
they always aggravate all the symptoms of an obstructed
circulation.[32] If the case be one of pre-existing disease of the
heart, they soon obliterate the cardiac cavities and lead to a rapid
fatal {727} termination. According to Grisolle,[33] when the
concretions are small and form an obstacle neither to the play of the
valves nor to the cardiac circulation, they are not revealed by any
appreciable functional trouble. The opinion of Grisolle in regard to
small coagula is also shared by Legroux, especially when they are fixed
at a distance from a cardiac orifice or concealed in a sinus. When,
however, the thrombi are larger and interfere more or less with the
course of the blood, they occasion very marked symptoms.
[Footnote 32: Hope, _On the Heart_, p. 486, Philada., 1846.]
[Footnote 33: _Pathologie interne_, p. 467, Paris, 1865.]
Even before the days of auscultation there were certain rational signs
which were dwelt upon with much force as showing the presence of
cardiac concretions. Thus, Senac[34] writes that the patients thus
afflicted feel a weight or oppression in the præcordial region which
sometimes becomes extremely painful. Palpitations and irregularities of
the pulse were also noted as symptomatic of these productions. Laennec
believes that coagula of any size may be recognized; "when, in a
patient who till then had presented regular pulsations of the heart,
these suddenly became so anomalous, confused, and obscure that they can
no longer be analyzed, we may suspect the formation of a polypous
concretion."[35] He further adds that if the trouble takes place on one
side alone of the heart, the fact is almost certain. When the coagula
occupy the cavities of the right heart, the sounds of the left heart
may remain normal whilst those of the right side are more or less
distant and muffled (Legroux). Several authors, amongst whom we should
mention Legroux, Bouillaud, Barth, and Roger, have mentioned amongst
the physical characters which show the existence of intra-cardiac
thrombi the sudden development of a blowing murmur limited to the
præcordial region or propagated into the aorta. Sometimes this bruit
was soft, sometimes harsh and rough. These writers have also noticed,
in conjunction with grave general symptoms, the doubling of the first
sound of the heart, making occasionally a sort of galloping murmur. As
regards the recognition of concretions on one side alone, I acknowledge
that after auscultating carefully several cases in which the autopsy
showed coagula formed during life, I have been unable to note signs
sufficient to justify a differential diagnosis.
[Footnote 34: _Traité de la Structure du Coeur, de son Action et de ses
Maladies_, t. ii. p. 470 _et suix_, quoted by Bucquoy.]
[Footnote 35: _De l'Auscult._, t. ii. p. 597, quoted by Hope.]